ArticleCurrent medical science2023
Liraglutide Suppresses Myocardial Fibrosis Progression by Inhibiting the Smad Signaling Pathway.
Article in Current medical science, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
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Who cites it
2 citing papers in PubMed, 2 citations in OpenAlex.
- The central role of IL-6 in the differential effects of GLP-1 receptor agonists and metformin across multiple health conditions.Frontiers in immunology · 2026Review
- High Hydrostatic Pressure Exacerbates Bladder Fibrosis through Activating Piezo1.Current medical science · 2024Article
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Authors and funding
5 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveLiraglutide is a commonly used hypoglycemic agent in clinical practice, and has been demonstrated to have protective effects against the development of cardiovascular disease. However, its potential role in myocardial fibrosis remains unexplored. The present study aims to assess the impact of liraglutide on the activation of cardiac fibroblasts.
methodsPrimary rat adult fibroblasts were isolated, cultured, and randomly allocated into 4 groups: control group, transforming growth factor beta1 (TGFβ1) stimulation group, liraglutide group, and TGFβ1+liraglutide group. Fibroblast activation was induced by TGFβ1. Cell proliferation activity was assessed using the CKK-8 kit, and cellular activity was determined using the MTT kit. Reverse transcrition-quantitative polymerase chain reaction (RT-qPCR) was utilized to quantify the level of collagen transcription, immunofluorescence staining was performed to detect the expression level of type III collagen and α-smooth muscle protein (α-SMA), and immunoblotting was conducted to monitor alterations in signal pathways.
resultsThe addition of 10, 25, 50 and 100 nmol/L of liraglutide did not induce any significant impact on the viability of fibroblasts (P>0.05). The rate of cellular proliferation was significantly higher in the TGFβl stimulation group than in the control group. However, the treatment with 50 and 100 nmol/L of liraglutide resulted in the reduction of TGFβl-induced cell proliferation (P<0.05). The RT-qPCR results revealed that the transcription levels of type I collagen, type III collagen, and α-SMA were significantly upregulated in the TGFβl stimulation group, when compared to the control group (P<0.05). However, the expression levels of these aforementioned factors significantly decreased in the TGFβl+liraglutide group (P<0.05). The immunofluorescence staining results revealed a significant increase in the expression levels of type III collagen and α-SMA in the TGFβl stimulation group, when compared to the control group (P<0.05). However, these expression levels significantly decreased in the TGFβl+liraglutide group, when compared to the TGFβl stimulation group (P<0.05). The Western blotting results revealed that the expression levels of phosphorylated smad2 and smad3 significantly increased in the TGFβl stimulation group, when compared to the control group (P<0.05), while these decreased in the TGFβl+liraglutide group (P<0.05).
conclusionLiraglutide inhibits myocardial fibrosis development by suppressing the smad signaling pathway, reducing the activation and secretion of cardiac fibroblasts.
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